Introduction
In December 2019, an outbreak of a coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) first emerged in Wuhan, China [1,2]. The World Health Organization declared a global pandemic on March 12, 2020, [3]. Since the first case was reported, COVID-19 has led to a significant increase in morbidity and mortality worldwide. The researchers are conducting several pharmacological studies against COVID-19 [4]. Among these research drugs, hydroxychloroquine (HQ), an antimalarial and anti-rheumatic drug, received wide attention at first. However, recently, its usage has remained in the background due to its side effect profile. We included the HQ in the study to prove that favipiravir’s arrhythmogenic effects were not inferior to HQ. Gautret et al. showed a significant reduction of the nasopharyngeal viral carriage in patients taking HQ [5]. Also, HQ inhibited SARS-CoV-2 activity in vitro [6]. The point to be considered is the relationship between QT prolongation with HQ [7]. Excessive prolongation of the QT interval may trigger Torsade de Pointes (TdP). TdP is a form of polymorphic ventricular tachycardia that can transform into ventricular fibrillation [8]. Furthermore, HQ directly contributes to myocardial suppression [9].
Favipiravir is a currently available drug being researched for COVID-19 treatment [10]. Essentially, favipiravir was approved for drug-resistant influenza treatment in 2014 in Japan [11]. It blocks viral replication by inhibiting the viral RNA-dependent RNA polymerase [12]. Therefore, favipiravir may also exert antiviral activity on SARS-CoV-2, an RNA virus. Recent studies have redesigned favipiravir to use in COVİD-19 treatment. In a recent in vitro study, Wang and colleagues found that favipiravir reduced viral replication [13]. A recent study demonstrated that favipiravir was associated with a shorter time to viral clearance and a higher recovery rate on chest scanning [14]. Chen et al. reported that favipiravir had a faster recovery period than umifenovir in COVID-19 patients [15]. Studies have reported that favipiravir is well tolerated and has a good safety profile [16,17]. Diarrhea, hyperuricemia, and elevated liver enzymes were the most frequent adverse effects reported in clinical trials [14,18]. Besides, Ghasemiyeh et al. revealed that favipiravir was infrequently associated with drug-induced psychotic symptoms [16]. Contrary to studies reporting that favipiravir has a well-established safety profile, we observed frequent conduction disorders in our patients. This study investigates the arrhythmogenic adverse effects of favipiravir in COVID-19 patients by comparing it with HQ, the best-known culprit in this regard.